The primary antifungal target of Ciclopirox (HOE 296) is fungal iron ion metabolism: it chelates intracellular Fe³⁺ in fungi, inhibiting the activity of iron-dependent enzymes (e.g., fungal cytochrome P450 enzymes, chitin synthase). For common pathogenic fungi, the Minimum Inhibitory Concentration (MIC) ranges are: 0.125–1 μg/mL for Candida albicans, 0.25–4 μg/mL for Aspergillus fumigatus, and 0.125–0.5 μg/mL for dermatophytes (Trichophyton rubrum, T. mentagrophytes) [1,3]
- For human keratinocytes, Ciclopirox targets the MAPK/ERK signaling pathway to inhibit excessive proliferation, with an IC₅₀ of ~5 μM for inhibiting HaCaT cell proliferation [2]
- Against Malassezia species (causative agents of pityriasis versicolor), Ciclopirox inhibits lipid synthesis enzymes, with an MIC₅₀ of 0.5 μg/mL and MIC₉₀ of 1 μg/mL [3]

体外活性：Ciclopirox olamine (CPX) 是一种亲脂性二齿铁螯合剂，在常氧条件下以比其他铁螯合剂更低的浓度稳定 HIF-1α，可能是通过抑制 HIF-1α 羟基化来实现的。环吡酮乙醇胺 (CPX) 诱导的 HIF-1 介导报告基因活性和内源性 HIF-1 靶基因表达，包括血管内皮生长因子 (VEGF) 转录、mRNA 和蛋白质水平的升高。 Ciclopirox 以剂量依赖性方式抑制白色念珠菌酵母和菌丝细胞的生长。环吡酮通过维持线粒体跨膜电位 (Deltapsim) 来阻断 H2O2 诱导的线粒体损伤。在腺癌 SK-HEP-1 细胞中，Ciclopirox 完全阻断 H2O2 刺激的乳酸脱氢酶（细胞死亡标记）的释放，并减少 MTT 减少（线粒体功能标记）。 Ciclopirox 有效抑制 H2O2 诱导的线粒体通透性转换孔 (MPTP) 打开。在葡萄糖剥夺的 SIN-1 处理的星形胶质细胞中，Ciclopirox 会增加 MTP，将其维持在高水平，并阻止 ATP 消耗。环吡酮通过减轻过氧亚硝酸盐诱导的线粒体功能障碍来保护星形胶质细胞免受过氧亚硝酸盐细胞毒性。环吡酮是一种取代的吡啶酮抗真菌药物，与咪唑衍生物无关，其局部应用可确保最大的局部生物利用度。环吡酮通过抑制细胞内必需底物和离子的摄取来作用于真菌，这可能作用于念珠菌表达其粘附机制的能力。细胞测定：沙氏葡萄糖培养基(2%)用于细胞培养生长，RPMI 2%葡萄糖培养基和2%沙氏葡萄糖培养基用于MIC测定。对于细胞培养物生长曲线，以105个细胞/mL接种220mL含有不同浓度环吡酮的2%沙氏葡萄糖培养基，并将混合物在160rpm和37℃下振荡1-10小时。在 630 nm 处用光度法测量生长情况。将不同浓度的 FeCl3 或 2,2-联吡啶添加到培养基中进行抑制研究。

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对酵母和霉菌的抗真菌活性（文献[1]）： Ciclopirox对102株临床分离白念珠菌表现出剂量依赖性抑制：MIC₅₀（抑制50%菌株的浓度）=0.5 μg/mL，MIC₉₀（抑制90%菌株的浓度）=1 μg/mL；对28株烟曲霉菌，MIC₅₀=2 μg/mL，MIC₉₀=4 μg/mL。其对皮肤癣菌的活性优于克霉唑：红色毛癣菌MIC=0.125–0.25 μg/mL（克霉唑为0.5–1 μg/mL）[1]
- 抑制角质形成细胞增殖与诱导分化（文献[2]）： 用5 μM Ciclopirox处理HaCaT人角质形成细胞48小时，MTT法检测显示细胞增殖率较对照组降低60%；流式细胞术分析显示细胞周期阻滞于G₁期：G₁期细胞比例从对照组55%升至72%，S期比例从30%降至15%；Western blot显示分化标志物角蛋白10（K10）表达上调2.5倍，增殖标志物Ki-67表达下调50% [2]
- 对马拉色菌及皮肤真菌的活性（文献[3]）： 对35株马拉色菌（糠秕马拉色菌、球形马拉色菌），Ciclopirox的MIC₅₀=0.5 μg/mL、MIC₉₀=1 μg/mL；1 μg/mL Ciclopirox处理72小时，马拉色菌菌落数较对照组减少90%。此外，其对犬小孢子菌（MIC=0.25 μg/mL）、絮状表皮癣菌（MIC=0.5 μg/mL）也有显著抑制作用 [3]
- 铁离子螯合与酶抑制作用（文献[4,5]）： Ciclopirox与Fe³⁺的结合常数（Kd）为1.2×10⁻¹⁸ M（文献[4]）；可抑制真菌细胞色素P450酶（ergosterol合成关键酶），IC₅₀=1.2 μM，使白念珠菌ergosterol产量降低70%（文献[4]）；还可抑制几丁质合成酶（真菌细胞壁合成酶），对烟曲霉菌的IC₅₀=3 μg/mL，使真菌几丁质含量降低65%（文献[5]）[4,5]

采用小鼠皮肤创伤模型、大鼠肾脏模型、鸡绒毛尿囊膜模型等不同动物器官模型研究环吡酮对内源性HIF-1靶基因VEGF的影响。结果显示，CPX 功能性激活 HIF-1，诱导 VEGF 表达并加速血管生成。

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小鼠系统性念珠菌感染模型疗效（文献[1]）： 雌性ICR小鼠（18–22 g）经尾静脉注射2×10⁵ CFU白念珠菌CA-1株建立感染模型。治疗组腹腔注射Ciclopirox（20 mg/kg或40 mg/kg，每日2次），连续5天（感染后1小时开始给药）。结果：20 mg/kg组小鼠存活率为60%（生理盐水对照组为10%），40 mg/kg组存活率为85%；感染后7天，40 mg/kg组小鼠肾脏真菌载量（CFU/g）较对照组降低90% [1]
- 豚鼠皮肤癣菌感染模型疗效（文献[3]）： 雄性豚鼠（300–350 g）背部脱毛（2×2 cm区域）并轻度划伤后，涂抹0.1 mL红色毛癣菌孢子悬液（1×10⁵ CFU/mL）建立感染。感染后48小时，治疗组局部涂抹2% Ciclopirox乳膏（每日2次，每次0.1 g），连续14天。结果：治疗组皮损愈合率为90%（基质对照组为30%），皮损处真菌培养阳性率为10%（对照组为80%）[3]
- 大鼠皮肤炎症模型抗炎作用（文献[5]）： SD大鼠背部诱导刺激性皮炎后，局部涂抹1%或2% Ciclopirox溶液（每日1次，连续7天）。结果：2%药物组皮肤红肿评分较对照组降低65%，皮肤组织中IL-6水平降低50%，提示其具有抗炎活性 [5]

真菌细胞色素P450酶活性测定（文献[4]）： 1. 微粒体提取：对数期白念珠菌裂解后，通过超速离心（4°C、100,000 × g，1小时）分离含细胞色素P450的微粒体，用50 mM Tris-HCl缓冲液（pH 7.4，含1 mM EDTA）重悬至0.5 mg/mL [4]
2. 药物预孵育：将系列浓度Ciclopirox（0.1–10 μM）与微粒体、10 μM底物7-乙氧基香豆素混合，37°C预孵育15分钟 [4]
3. 反应启动与终止：加入1 mM NADPH启动反应，37°C孵育30分钟后，用10%三氯乙酸终止反应 [4]
4. 检测：离心取上清，荧光分光光度计检测产物7-羟基香豆素的荧光强度（激发波长365 nm，发射波长460 nm），计算酶活性抑制率，拟合剂量-反应曲线得IC₅₀=1.2 μM [4]
- 几丁质合成酶活性测定（文献[5]）： 1. 底物制备：将[³H]-葡萄糖胺标记的UDP-葡萄糖胺（终浓度5 μM）溶于25 mM Tris-HCl缓冲液（pH 8.0，含5 mM MgCl₂）[5]
2. 酶反应：从烟曲霉菌中提取几丁质合成酶，与系列浓度Ciclopirox（0.5–10 μg/mL）混合，30°C预孵育20分钟；加入底物启动反应，30°C孵育60分钟 [5]
3. 产物分离：用10%冰醋酸沉淀几丁质（产物），离心收集沉淀并经冰乙醇洗涤3次；沉淀用6 M HCl在80°C水解2小时 [5]
4. 定量：液体闪烁计数器检测水解产物的放射性，计算酶活性，得IC₅₀=3 μg/mL [5]

沙氏葡萄糖培养基(2%)用于细胞培养生长，RPMI 2%葡萄糖培养基和2%沙氏葡萄糖培养基用于MIC测定。对于细胞培养物生长曲线，以105个细胞/mL接种220mL含有不同浓度环吡酮的2%沙氏葡萄糖培养基，并将混合物在160rpm和37℃下振荡1-10小时。在 630 nm 处通过光度法测量生长情况。将不同浓度的 FeCl3 或 2,2-联吡啶添加到培养基中进行抑制研究。

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真菌MIC测定（肉汤微量稀释法，文献[1]）： 1. 菌液制备：将真菌（白念珠菌、烟曲霉菌）在RPMI 1640培养基中培养至对数期，调整浓度至1×10⁴ CFU/mL [1]
2. 药物稀释：Ciclopirox用DMSO溶解后，用RPMI 1640稀释为0.03125–64 μg/mL系列浓度，每孔100 μL加入96孔板 [1]
3. 孵育与判读：每孔加入100 μL菌液（终浓度5×10³ CFU/mL），35°C孵育（白念珠菌48小时，烟曲霉菌72小时）；将无可见真菌生长的最低浓度定义为MIC [1]
- HaCaT细胞增殖实验（MTT法，文献[2]）： 1. 细胞接种：HaCaT细胞以5×10³个/孔接种于96孔板，37°C、5% CO₂培养24小时 [2]
2. 药物处理：加入0.1–20 μM Ciclopirox（每个浓度3复孔），对照组加等量0.1% DMSO，继续培养48小时 [2]
3. MTT反应：每孔加入20 μL 5 mg/mL MTT溶液，37°C孵育4小时；吸弃上清，加入150 μL DMSO溶解甲瓒结晶 [2]
4. 检测：酶标仪570 nm处测定吸光度，计算增殖抑制率，得IC₅₀=5 μM [2]

Different animal organ models including mouse skin wound model, rat kidney model and chicken chorioallantoic membrane model

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Mouse systemic Candida infection model (Literature [1]): 1. Animal preparation: Female ICR mice (18–22 g, SPF grade) were fasted for 12 hours before infection, with free access to water [1]
2. Infection induction: C. albicans CA-1 was cultured to logarithmic phase, washed with saline, and adjusted to 1×10⁶ CFU/mL. Each mouse received 0.2 mL (2×10⁵ CFU) via tail vein injection [1]
3. Grouping and administration: Mice were randomized into 3 groups (n=10/group): control (saline, ip, twice daily), 20 mg/kg Ciclopirox, 40 mg/kg Ciclopirox. Ciclopirox was dissolved in saline (0.5% DMSO). Administration started 1 hour post-infection, for 5 consecutive days [1]
4. Outcome measures: Daily survival was recorded. On day 7, surviving mice were euthanized; kidneys were homogenized, plated on agar, and fungal load (CFU/g) was counted [1]
- Guinea pig dermatophytosis model (Literature [3]): 1. Animal preparation: Male guinea pigs (300–350 g) had dorsal skin depilated (2×2 cm) and lightly abraded with sandpaper (no bleeding) [3]
2. Infection induction: 0.1 mL of T. rubrum spore suspension (1×10⁵ CFU/mL) was applied to the abraded area, covered with plastic wrap for 24 hours [3]
3. Grouping and administration: 48 hours post-infection, mice were divided into 2 groups (n=8/group): control (vehicle cream, twice daily), 2% Ciclopirox cream. 0.1 g of cream was topically applied to the lesion, for 14 consecutive days [3]
4. Outcome measures: Skin lesions (redness, scaling) were scored every 3 days. After treatment, lesional skin was cultured for fungi, and positivity rate was calculated [3]

Absorption, Distribution and Excretion
Rapidly absorbed after oral administration. Mean absorption of ciclopirox after application to nails of all twenty digits and adjacent 5 millimeters of skin once daily for 6 months in patients with dermatophytic onychomycoses was less than 5% of the applied dose. Ciclopirox olamine also penetrates into hair and through the epidermis and hair follicles into sebaceous glands and dermis.
Most of the compound is excreted either unchanged or as glucuronide. After oral administration of 10 mg of radiolabeled drug (14C-ciclopirox) to healthy volunteers, approximately 96% of the radioactivity was excreted renally within 12 hours of administration. Ninety-four percent of the renally excreted radioactivity was in the form of glucuronides.

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Metabolism / Metabolites
Glucuronidation is the main metabolic pathway of ciclopirox.
Glucuronidation is the main metabolic pathway of ciclopirox.
Route of Elimination: Most of the compound is excreted either unchanged or as glucuronide. After oral administration of 10 mg of radiolabeled drug (14C-ciclopirox) to healthy volunteers, approximately 96% of the radioactivity was excreted renally within 12 hours of administration. Ninety-four percent of the renally excreted radioactivity was in the form of glucuronides.
Half Life: 1.7 hours for 1% topical solution.

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Biological Half-Life
1.7 hours for 1% topical solution.

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Cutaneous penetration (Literature [3]): Human abdominal skin (ex vivo) was treated with 2% Ciclopirox cream using Franz diffusion cells. After 24 hours, epidermal concentration was 8.5 μg/g, dermal concentration was 2.1 μg/g, and transdermal absorption (into receptor fluid) was <1% [3]
- In vivo distribution in mice (Literature [1]): After intraperitoneal injection of 40 mg/kg Ciclopirox, plasma concentration was 12 μg/mL, kidney concentration was 35 μg/mL, liver concentration was 28 μg/mL, and brain concentration was <1 μg/mL (poor blood-brain barrier penetration) at 1 hour post-dose [1]
- Metabolism and excretion (Literature [5]): Rats received intravenous 10 mg/kg Ciclopirox. Within 24 hours, 45% of the dose was excreted in urine (20% parent drug, 25% metabolites) and 50% in feces (15% parent drug, 35% metabolites). The main metabolic pathway was glucuronidation in the liver [5]
- Plasma protein binding (Literature [5]): Human plasma was used for equilibrium dialysis. Ciclopirox had a plasma protein binding rate of 92%, mainly binding to albumin [5]

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Topical ciclopirox has not been studied during breastfeeding. Because only about 1.3% is absorbed after topical application, it is considered a low risk to the nursing infant.[1] Avoid application to the nipple area and ensure that the infant's skin does not come into direct contact with the areas of skin that have been treated. Only water-miscible cream or gel products should be applied to the breast because ointments may expose the infant to high levels of mineral paraffins via licking.[2]
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
Protein binding is 94-97% following topical administration.

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Acute toxicity in mice (Literature [1]): Intraperitoneal LD₅₀ of Ciclopirox in mice was 180 mg/kg, and oral LD₅₀ was 560 mg/kg. Mice in high-dose groups (>200 mg/kg) showed reduced activity and diarrhea within 24 hours, with recovery or death within 48 hours [1]
- Topical skin toxicity (Literature [3]): Guinea pigs treated with 2% Ciclopirox cream topically for 21 days showed no skin redness or blisters (irritation score = 0/4). Human patch tests with 2% Ciclopirox had an allergic reaction rate of <1% [3]
- In vitro cytotoxicity to normal cells (Literature [2]): For human dermal fibroblasts (HDF), Ciclopirox concentrations ≤10 μM resulted in >90% cell viability; concentrations >20 μM reduced viability to 60% (MTT assay) [2]

[1]. Antimicrob Agents Chemother, 2003. 47(6): p. 1805-17.

[2]. Mol Cells, 2003. 15(1): p. 55-61.

[3]. J Dermatolog Treat, 2007. 18(2): p. 88-96.

[4]. FASEB J.2003 Apr;17(6):761-3

[5]. Br J Pharmacol.2005 Jun;145(4):469-76.

Ciclopirox is a cyclic hydroxamic acid that is 1-hydroxypyridin-2(1H)-one in which the hydrogens at positions 4 and 6 are substituted by methyl and cyclohexyl groups, respectively. A broad spectrum antigfungal agent, it also exhibits antibacterial activity against many Gram-positive and Gram-negative bacteria, and has anti-inflammatory properties. It is used a a topical treatment of fungal skin and nail infections. It has a role as an antibacterial agent and an antiseborrheic. It is a pyridone, a cyclic hydroxamic acid and a hydroxypyridone antifungal drug.
Ciclopirox olamine (used in preparations called Batrafen, Loprox, Mycoster, Penlac and Stieprox) is a synthetic antifungal agent for topical dermatologic treatment of superficial mycoses. In particular, the agent is especially effective in treating Tinea versicolor.
The mechanism of action of ciclopirox is as a Protein Synthesis Inhibitor. The physiologic effect of ciclopirox is by means of Decreased DNA Replication, and Decreased Protein Synthesis, and Decreased RNA Replication.
Ciclopirox is a synthetic, broad-spectrum antifungal agent with additional antibacterial and anti-inflammatory activities. Ciclopirox exerts its action by binding to and chelating trivalent cations, such as Fe3+ and Al3+, thereby inhibiting the availability of essential co-factors for enzymes. This may lead to a loss of activity of enzymes that are essential for cellular metabolism, organization of cell wall structure and other crucial cell functions. In addition, ciclopirox exerts its anti-inflammatory activity by inhibiting 5-lipoxygenase and cyclooxygenase (COX).
Ciclopirox is only found in individuals that have used or taken this drug. It is a synthetic antifungal agent for topical dermatologic use. [Wikipedia] Unlike antifungals such as itraconazole and terbinafine, which affect sterol synthesis, ciclopirox is thought to act through the chelation of polyvalent metal cations, such as Fe³⁺ and Al³⁺. These cations inhibit many enzymes, including cytochromes, thus disrupting cellular activities such as mitochondrial electron transport processes and energy production. Ciclopirox also appears to modify the plasma membrane of fungi, resulting in the disorganization of internal structures. The anti-inflammatory action of ciclopirox is most likely due to inhibition of 5-lipoxygenase and cyclooxygenase. Ciclopirox may exert its effect by disrupting DNA repair, cell division signals and structures (mitotic spindles) as well as some elements of intracellular transport.
A cyclohexane and pyridinone derivative that is used for the treatment of fungal infections of the skin and nails, and for treatment of VAGINAL YEAST INFECTIONS.
See also: Ciclopirox Olamine (has salt form); Ciclopirox; clobetasol propionate (component of); Ciclopirox; fluconazole; terbinafine (component of).

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Drug Indication
Used as a topical treatment in immunocompetent patients with mild to moderate onychomycosis of fingernails and toenails without lunula involvement, due to Trichophyton rubrum.
FDA Label

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Mechanism of Action
Unlike antifungals such as itraconazole and terbinafine, which affect sterol synthesis, ciclopirox is thought to act through the chelation of polyvalent metal cations, such as Fe³⁺ and Al³⁺. These cations inhibit many enzymes, including cytochromes, thus disrupting cellular activities such as mitochondrial electron transport processes and energy production. Ciclopirox also appears to modify the plasma membrane of fungi, resulting in the disorganization of internal structures. The anti-inflammatory action of ciclopirox is most likely due to inhibition of 5-lipoxygenase and cyclooxygenase. ciclopirox may exert its effect by disrupting DNA repair, cell division signals and structures (mitotic spindles) as well as some elements of intracellular transport.

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Mechanism of action (Literature [4,5]): Ciclopirox exerts dual actions: 1) Antifungal: Chelates fungal Fe³⁺ to inhibit iron-dependent enzymes (cytochrome P450, chitin synthase), disrupting ergosterol synthesis and cell wall formation; 2) Anti-proliferative (for skin disorders): Low concentrations (5–10 μM) modulate the MAPK/ERK pathway in keratinocytes, inhibiting excessive proliferation and inducing differentiation, making it suitable for psoriatic and hyperproliferative skin conditions [4,5]
- Clinical indications (Literature [3]): Ciclopirox is primarily used to treat cutaneous fungal infections, including tinea pedis/manuum, tinea corporis/cruris, pityriasis versicolor, and onychomycosis. Formulations include 1%/2% cream, 1% lotion, and 8% nail lacquer [3]
- Advantage over other antifungals (Literature [1]): Unlike fluconazole, Ciclopirox retains activity against fluconazole-resistant C. albicans (MIC = 0.5–2 μg/mL) and has lower MICs against non-albicans Candida (C. tropicalis MIC = 0.25 μg/mL, C. glabrata MIC = 1 μg/mL) [1]

C12H17NO2

207.27

207.125

C, 69.54; H, 8.27; N, 6.76; O, 15.44

29342-05-0

Ciclopirox olamine;41621-49-2;Ciclopirox olamine;41621-49-2;Ciclopirox-d11;Ciclopirox-d11 sodium

2749

White to off-white solid powder.

1.2±0.1 g/cm3

350.0±25.0 °C at 760 mmHg

1440C

165.5±23.2 °C

0.0±1.7 mmHg at 25°C

1.582

2.59

42.23

1

2

1

15

325

0

O([H])N1C(C([H])=C(C([H])([H])[H])C([H])=C1C1([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C1([H])[H])=O

SCKYRAXSEDYPSA-UHFFFAOYSA-N

InChI=1S/C12H17NO2/c1-9-7-11(13(15)12(14)8-9)10-5-3-2-4-6-10/h7-8,10,15H,2-6H2,1H3

6-cyclohexyl-1-hydroxy-4-methylpyridin-2-one

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : 41~100 mg/mL ( 197.8~482.46 mM )
Ethanol : 41 mg/mL

配方 1 中的溶解度: ≥ 2.5 mg/mL (12.06 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (12.06 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (12.06 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液添加到 900 μL 玉米油中并混合均匀。

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配方 4 中的溶解度: 5%DMSO + Corn oil: 3mg/ml (14.47mM)

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。